Frequently Asked Questions about Lowered Life Expectancy for Women, Obesity and the Environment

A recent study in the journal PLoS Medicine (Ezzati et al. 2008) concluded that in nearly 1,000 counties in America, which are home to about 12 percent of the nation's women, life expectancy became shorter by 1999 than it was in the early 1980s. Although life span has generally increased since 1961, the authors reported it began to level off or even decline in the 1980s for 4 percent of men and 19 percent of women.

• To what do the researchers attribute this drop in life expectancy in women up to 1999?
• Why was this study conducted?
• Did data reveal differences between disadvantaged and advantaged populations in gains in life expectancy?
• What were some of the geographic disparities found?
• What did researchers notice about overweight or obesity trends in men and women?
• How could the environment play a role in obesity?
• Diabesity trends
• What recent scientific literature has been published on ‘obesogens’?
• What is now known about aspartame and obesity?
• What is the evidence for the link between endocrine-disrupting chemicals and obesity?
• In regards to bisphenol A, what is prudent public policy?
• References

To what do the researchers attribute this drop in life expectancy in women up to 1999?

Findings indicate that women have been dying increasingly from diabetes, lung cancer, emphysema, and kidney failure, reflecting the long-term consequences of smoking. Unfortunately, women took up this habit in large numbers decades after men did. The authors also found that this may represent the leading edge of the obesity epidemic. If so, women's life expectancy could decline broadly across the United States in coming years.

Why was this study conducted?

The researchers examined mortality and cause-of-death data for the United States from 1961 through 1999 to see whether there were different life expectancies across different U.S. counties over the last four decades. The researchers chose to look at counties—the smallest geographic units for which data on death rates are collected in the US—because it allowed them to make comparisons between small subgroups of people.

Did data reveal differences between disadvantaged and advantaged populations in gains in life expectancy?

Yes. The findings suggest that beginning in the early 1980s and continuing through 1999, disadvantaged populations did not experience the same gains in life expectancy experienced by advantaged populations, and some became even worse off. In those counties, life expectancy increased by only one year (from 74.5 to 75.5 years) between 1983 and 1999, while in the advantaged counties, life expectancy of women reached 83 years. Unfortunately, this growing disparity in women's mortality is tied in with race, income and geography. For instance, in counties where were more African-Americans lived, life expectancy declined the most.

What were some of the geographic disparities found?

Counties with significant declines in women's life expectancies were concentrated in Appalachia, the Southeast, Texas, the southern Midwest and along the Mississippi River. Life expectancy increases were seen mainly in the Northeast and on the Pacific Coast. The study found that after 1983, life span rose with wealth.

What did researchers notice about overweight or obesity trends in men and women?

Obesity has risen markedly in the past two decades, with women more affected than men. About 33 percent of women are now obese, compared with 31 percent of men, and extreme obesity is twice as common in women (7 percent) as in men (3 percent). High blood pressure, which can be partly attributed to weight gain, has been increasing in women and declining in men. In 1990, 2 out of every 5 women over 60 had hypertension and by 2000, it was one out of every two. Being overweight also greatly increases the risk of developing Type 2, or "adult onset" diabetes.

How could the environment play a role in obesity?

This relationship is currently being examined within the scientific community. Research on the obesity epidemic in the United States over the last few decades is being conducted around such environmental factors as: 1.) aspartame and other artificial sweeteners that can stimulate appetite and obesity; and 2.) endocrine disrupting chemicals (such as those found in plasticizers and personal care products) and obesogens (chemicals that have been shown to cause obesity in animals). In cancer research, every chemical that we can prove causes cancer in humans also causes cancer in animals, when adequately studied. Therefore, we have reason to suspect that chemicals which cause obesity in animals may also cause obesity in humans.

Recently, researchers showed that when Agouti mice (mice that are all genetically-related) were fed prenatal diets high in BPA (a hormone-disrupting chemical found, for instance, in some plastics and the linings of some canned goods), those mice became obese—twice the weight of a normal mouse—and had increased risk of breast and prostate cancers(Dolinoy et al. 2007a). This finding has led scientists to develop the Environmental Obesogens / Diabesity Hypothesis: Pre-natal, early life and young life exposures to bisphenol A (BPA) activate fat receptors and stimulate fat cells, which predispose individuals to obesity and/or related metabolic disorders (diabesity).

Diabesity trends:

• More than 20% of adults are clinically obese.
• An additional 30% are defined as overweight.
• In 1999, 13% of children aged 6–11 years and 14% of adolescents aged 12–19 years in the United States.
• The rate of obesity has doubled in past decade, now 30% of all adults.

Genetically identical agouti mice, one fed a diet of bisphenol A (BPA) (Dolinoy et al. 2007b).

What recent scientific literature has been published on ‘obesogens’?

(Arsenescu, et al. 2008) A widely used flame retardant, PCB 77, causes increased body weight and ‘bad’ cholesterol when exposed at low levels, but reduces body weight at much higher levels.  Some cancers are associated with obesity. Additional research should consider whether different PCB exposures are associated with obesity are also associated with cancer. That would assist national cancer organizations currently concerned with obesity and cancer in recognizing that more than lifestyle and the built environment are associated with obesity and its known cancer risks.
-- Michael Lerner, PhD, President, Commonweal and Founding CHE (The Collaborative on Health and the Environment) Partner

For more information contact:

Lisa Cassis, Ph.D. - Professor & Chair
Graduate Center for Nutritional Sciences
Room 521B, Wethington Building
University of Kentucky
Lexington, KY 40536-0200
Tel: 859-323-4933 (ext. 81400)
LCassis@uky.edu

To learn more about this project, please refer to the following sources:

What is now known about aspartame and obesity?

Aspartame is consumed by about 200 million Americans every day. In America today, more than ten million children regularly consume diet sodas and other foods containing aspartame. The greater vulnerability of the young to carcinogens has consistently been demonstrated experimentally in aspartame and a number of other compounds. Experiments conducted in 2008 by an Italian research group, found that animals exposed prenatally to aspartame have double the risk of developing multiple tumors compared with animals exposed postnatally (Soffritti et al. 2008). In light of these findings, when evaluating public health impacts of widely-used materials, it is important to consider the effect of exposures over a lifetime, especially those that may begin prenatally.

What is the evidence for the link between endocrine-disrupting chemicals and obesity?

A recent study found that prenatal exposure to organotins (a diverse group of widely distributed chemical pollutants) demonstrated that these chemicals disrupt the delicate signaling path of hormones and therefore could lie behind the growing obesity epidemic (Grün et al. 2006). In utero exposure to these persistent, widespread pollutants can elevate fat found in the liver and testis. The animals, once born, also were fatter. These organotins pollutants may be contributing to, in part, the obesity epidemic. Research is ongoing on these important new findings.

In regards to bisphenol A, what is prudent public policy?

Michael Thun, of the American Cancer Society, stated that limiting exposure to BPA is "prudent." (American Cancer Society 2008)

The U.S. National Institute of Environmental Health Sciences suggests following these steps to reduce BPA exposure (National Institute of Environmental Health Sciences 2008)::

• Don't microwave polycarbonate plastic food containers. Polycarbonate is strong and durable, but over time it may break down from over use at high temperatures.
• Polycarbonate containers that contain BPA usually have a #7 on the bottom
• Reduce your use of canned foods.
• When possible, opt for glass, porcelain or stainless steel containers, particularly for hot food or liquids.
• Use baby bottles that are BPA free.

See The National Toxicology Program (NTP) Draft Brief On Bisphenol A (BPA) for detailed information and recommendations (National Toxicology Program 2008).

References

1. American Cancer Society. Science Daily. 2008 22 April. Chemical in Plastic Bottles Raises some Concern, According to New Report. Accessed 2008 25 April.
2. Arsenescu V., R.I. Arsenescu, V. King, H. Swanson, and L.A. Cassis. In Press (Available on-line). Polychlorinated Biphenyl 77 Induces Adipocyte Differentiation and Proinflammatory Adipokines and Promotes Obesity and Atherosclerosis. Environmental Health Perspectives.
3. Bakalar N. 2008. Life expectancy is declining in some pockets of the country. New York Times April 22, 2008, F:5.
4. Brown D. 2008. Life expectancy drops for some U.S. women: Historic reversal, found in 1,000 counties, may be result of smoking and obesity. The Washington Post April 22, 2008, A:1.
5. Dolinoy DC, Huang D, Jirtle RL. 2007a. Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proceedings of the National Academy of Sciences of the United States of America 104(32): 13056-61.
6. Dolinoy DC, Weidman JR, Jirtle RL. 2007b. Epigenetic gene regulation: Linking early developmental environment to adult disease. Reproductive Toxicology 23(3): 297-307.
7. Ezzati M, Friedman AB, Kulkarni SC, Murray, Christopher J. L. 2008. The reversal of fortunes: Trends in county mortality and cross-county mortality disparities in the United States. PLoS Medicine 5(4): 557-68.
8. Grün F, Watanabe H, Zamanian Z, Maeda L, Arima K, Cubacha R, Gardiner DM, Kanno J, Iguchi T, Blumberg B. 2006. Endocrine-disrupting organotin compounds are potent inducers of adipogenesis in vertebrates. Molecular Endocrinology 20(9): 2141-55
9. National Institute of Environmental Health Sciences and National Toxicology Program. 2008 April 14. Since You Asked - Bisphenol A: Questions and Answers about the Draft National Toxicology Program Brief on Bisphenol A. Accessed 2008 April 25.
10. National Toxicology Program. 2008. Draft NTP brief on bisphenol A.
11. Soffritti M, Belpoggi F, Esposti DD, Falcioni L, Bua L. 2008. Consequences of exposure to carcinogens beginning during developmental life. Basic & Clinical Pharmacology & Toxicology 102(2): 118-24.

To inquire about Center for Environmental Oncology activities, please send an e-mail to envonc@upmc.edu or call 412-623-3375.